71 research outputs found

    Cell culture device using spatial light modulator

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    Spatial light modulator is introduced for cell culturing and related illumination experiment. Two kinds of designs were used. The first type put the cell along with the bio-medium directly on top of the analyzer of the microdisplay and set a cover glass on it to retain the medium environment, which turned the microdisplay into a bio-container. The second type introduced an optical lens system placed below the spatial light modulator to focus the light spots on specific position. Details of the advantages and drawbacks for the two different approaches are discussed, and the human melanocyte cell (HMC) is introduced to prove the feasibility of the concept. Results indicate that the second type is much more suitable than the first for precision required application

    Pulse-mode quantum projection synthesis: Effects of mode mismatch on optical state truncation and preparation

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    Quantum projection synthesis can be used for phase-probability-distribution measurement, optical-state truncation and preparation. The method relies on interfering optical lights, which is a major challenge in experiments performed by pulsed light sources. In the pulsed regime, the time frequency overlap of the interfering lights plays a crucial role on the efficiency of the method when they have different mode structures. In this paper, the pulsed mode projection synthesis is developed, the mode structure of interfering lights are characterized and the effect of this overlap (or mode match) on the fidelity of optical-state truncation and preparation is investigated. By introducing the positive-operator-valued measure (POVM) for the detection events in the scheme, the effect of mode mismatch between the photon-counting detectors and the incident lights are also presented.Comment: 11 pages, 4 figures, submitted to Phys. Rev.

    Multipartite Entanglement and Quantum State Exchange

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    We investigate multipartite entanglement in relation to the theoretical process of quantum state exchange. In particular, we consider such entanglement for a certain pure state involving two groups of N trapped atoms. The state, which can be produced via quantum state exchange, is analogous to the steady-state intracavity state of the subthreshold optical nondegenerate parametric amplifier. We show that, first, it possesses some 2N-way entanglement. Second, we place a lower bound on the amount of such entanglement in the state using a novel measure called the entanglement of minimum bipartite entropy.Comment: 12 pages, 4 figure

    Glial activation involvement in neuronal death by Japanese encephalitis virus infection

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    Japanese encephalitis is characterized by profound neuronal destruction/dysfunction and concomitant microgliosis/astrogliosis. Although substantial activation of glia is observed in Japanese encephalitis virus (JEV)-induced Japanese encephalitis, the inflammatory responses and consequences of astrocytes and microglial activation after JEV infection are not fully understood. In this study, infection of cultured neurons/glia with JEV caused neuronal death and glial activation, as evidenced by morphological transformation, increased cell proliferation and elevated tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 and RANTES (regulated upon activation, normal T-cell expressed and secreted) production. Replication-competent JEV caused all glial responses and neurotoxicity. However, replication-incompetent JEV lost these abilities, except for the ability to change microglial morphology. The bystander damage caused by activated glia also contributed to JEV-associated neurotoxicity. Microglia underwent morphological changes, increased cell proliferation and elevated TNF-alpha, IL-1 beta, IL-6 and RANTES expression in response to JEV infection. In contrast, IL-6 and RANTES expression, but no apparent morphological changes, proliferation or TNF-alpha/IL-1 beta expression, was demonstrated in JEV-infected astrocytes. Supernatants of JEV-infected microglia, but not JEV-infected astrocytes, induced glial activation and triggered neuronal death. Antibody neutralization studies revealed that TNF-alpha and IL-1 beta, but not RANTES or IL-6, released by activated microglia appeared to play roles in JEV-associated neurotoxicity. In conclusion, following JEV infection, neuronal death was accompanied by concomitant microgliosis and astrogliosis, and neurotoxic mediators released by JEV-activated microglia, rather than by JEV-activated astrocytes, had the ability to amplify the microglial response and cause neuronal death

    Space Telescope and Optical Reverberation Mapping Project. VII. Understanding the Ultraviolet Anomaly in NGC 5548 with X-Ray Spectroscopy

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    During the Space Telescope and Optical Reverberation Mapping Project observations of NGC 5548, the continuum and emission-line variability became decorrelated during the second half of the six-month-long observing campaign. Here we present Swift and Chandra X-ray spectra of NGC 5548 obtained as part of the campaign. The Swift spectra show that excess flux (relative to a power-law continuum) in the soft X-ray band appears before the start of the anomalous emission-line behavior, peaks during the period of the anomaly, and then declines. This is a model-independent result suggesting that the soft excess is related to the anomaly. We divide the Swift data into on- and off-anomaly spectra to characterize the soft excess via spectral fitting. The cause of the spectral differences is likely due to a change in the intrinsic spectrum rather than to variable obscuration or partial covering. The Chandra spectra have lower signal-to-noise ratios, but are consistent with the Swift data. Our preferred model of the soft excess is emission from an optically thick, warm Comptonizing corona, the effective optical depth of which increases during the anomaly. This model simultaneously explains all three observations: the UV emission-line flux decrease, the soft-excess increase, and the emission-line anomaly

    Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

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    A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk

    The Immune Landscape of Cancer

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    We performed an extensive immunogenomic anal-ysis of more than 10,000 tumors comprising 33diverse cancer types by utilizing data compiled byTCGA. Across cancer types, we identified six im-mune subtypes\u2014wound healing, IFN-gdominant,inflammatory, lymphocyte depleted, immunologi-cally quiet, and TGF-bdominant\u2014characterized bydifferences in macrophage or lymphocyte signa-tures, Th1:Th2 cell ratio, extent of intratumoral het-erogeneity, aneuploidy, extent of neoantigen load,overall cell proliferation, expression of immunomod-ulatory genes, and prognosis. Specific drivermutations correlated with lower (CTNNB1,NRAS,orIDH1) or higher (BRAF,TP53,orCASP8) leukocytelevels across all cancers. Multiple control modalitiesof the intracellular and extracellular networks (tran-scription, microRNAs, copy number, and epigeneticprocesses) were involved in tumor-immune cell inter-actions, both across and within immune subtypes.Our immunogenomics pipeline to characterize theseheterogeneous tumors and the resulting data areintended to serve as a resource for future targetedstudies to further advance the field

    Suppression of promoter activity of the LAT gene by IE180 of pseudorabies virus

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    The latency-associated transcript (LAT) gene is the only viral genomic region that is abundantly transcribed during pseudorabies virus (PrV) latent infection. The mechanism of reactiviation of PrV from latency remains unknown. To analyze the regulation mechanism of the LAT promoter, we constructed a series of recombinant vectors in which various sequences upstream of LAT were linked to the chloramphenicol acetyltransferase (CAT) gene. Transcriptional efficiency was examined by cotransfection with plasmids carrying the PrV IE, EPO, or gD gene, respectively. Results showed that the activity of PrV LAT promoter was dramatically repressed by the IE180 protein and a TATA box and a putative IE180 binding site within the promoter were involved in this repression. To dissect the functional domains of IE180, we compared the relative repressive abilities of IE180 variants to the LAT promoter by transient transfection assays. Mutational analysis demonstrated that almost the whole IE180 (amino acid residues 1-1440) are essential for its repression to the LAT promoter. To explore the possible mechanism of repression, an electrophoretic mobility shift assay (EMSA) using nuclear extracts from neuronal cells was performed and formation of protein-DNA complexes between IE180 and the oligonucleotide probed (-46 to -19, relative to the start site of LAT transcription) was demonstrated. The association of IE180 with the region encompassing the putative IE180 binding site and the TATA box upstream of PrV LAT gene was further confirmed by supershift of EMSA complexes using IE180 specific antibody. Thus, our results suggested that IE180 repressed the LAT promoter via an interaction between IE180, LAT promoter and cellular proteins

    A TEF-1-element is required for activation of the promoter of pseudorabies virus glycoprotein X gene by IE180

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    The pseudorabies virus (PRV) immediate-early regulatory protein IE180 is able to transactivate the viral early and late genes. Using chloramphenicol acetyltransferase (CAT) assay, we investigated the transactivation function of IE180 to the promoter of PRV glycoprotein X (gX) gene, and our results showed that IE180 could significantly increase the expression of CAT gene which was under the control of gX promoter. To further identify the activation domains of IE180 protein that interact with the gX promoter sequences, various truncated mutants of IE180 gene and gX promoter gene were constructed and analyzed by CAT and gel retardation assay. Results revealed that the N-terminal amino acid residues from 133 to 736 of IE180 could interact with the binding site of transcriptional enhancer factor-1 (TEF-1) that resides in the gX promoter. Formation of protein-DNA complexes between the IE180 protein and the TEF-1 element of the gX promoter was observed using electrophoretic mobility shift assay (EMSA) as well as Southwestern blot analysis. These results indicated that a direct interaction occurred between IE180 and the TEF-1 element; and this interaction was abolished in the TEF-1 element was mutated. The association of IE180 with the TEF-1 element was further confirmed by the supershift of EMSA complexes using IE180 specific antibody. Taken together, our results suggested that formation of a complex between the IE180 protein and TEF-1 element in the gX promoter region was involved in the transcriptional regulation of the gX gene
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